Leukotriene antagonists and Churg-Strauss syndrome: the smoking gun

Stirling, Robert; Chung, KF

doi:10.1136/thx.54.10.865

Cited by 38 publications

(20 citation statements)

References 23 publications

(20 reference statements)

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“…[52][53][54][55] Indeed, almost all cases suggested a temporal relationship between LTRA use and CSS onset, but without the demonstration or exclusion of a potential direct role.…”

Section: Relationships Between Lma Use and Css Development: The Diffementioning

confidence: 99%

Churg-Strauss Syndrome and Leukotriene-Modifying Agents

Pagnoux¹,

Guilpain²,

Hauser³

et al. 2004

Clinical Pulmonary Medicine

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Churg-Strauss syndrome (CSS) is a primary systemic necrotizing vasculitis of unknown origin, which is typically characterized by the association of asthma and blood eosinophilia. Leukotriene-modifying agents include zileuton, a 5-lipoxygenase inhibitor, and 3 selective leukotriene type 1 receptor antagonists (LTRA: zafirlukast, montelukast, and pranlukast) that have all been approved for the treatment of persistent asthma. Since 1996, when the first LTRA became available, more than 100 cases of CSS possibly related to LTRA use have been recorded by the US Food and Drug administration, and more than 50 cases have been described in the literature. These CSS developed 2 days to 15 months after LTRA introduction. Their clinical and biologic manifestations were similar to those of CSS occurring independently of LTRA use; however, the former may develop more often cardiomyopathy, but neuropathy and anticytoplasmic autoantibodie positivity less frequently than in the latter form of CSS. Notably, outcome after LTRA discontinuation and under systemic steroid therapy was usually good. These cases of CSS may result from the unmasking of an underlying incipient "forme fruste" of the vasculitis, during the steroid withdrawal or tapering made possible by LTRA therapy, or from a direct causal role of LTRA. Pertinently, these hypotheses are not exclusive and, until further studies clarify this point, the wisest strategy seems to be to discontinue or avoid their use in CSS patients, to carefully monitor asthmatic patients taking these drugs and to remember that CSS onset may resemble a worsening of persistent mild or severe asthma.

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“…[52][53][54][55] Indeed, almost all cases suggested a temporal relationship between LTRA use and CSS onset, but without the demonstration or exclusion of a potential direct role.…”

Section: Relationships Between Lma Use and Css Development: The Diffementioning

confidence: 99%

Churg-Strauss Syndrome and Leukotriene-Modifying Agents

Pagnoux¹,

Guilpain²,

Hauser³

et al. 2004

Clinical Pulmonary Medicine

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“…A few cases of the syndrome have also been described after zafirlukast in patients not receiving systemic steroid treatment [12]. The high incidence of such a rare entity [11] during the commercial postmarketing surveillance of cysteinyl LT 1 receptor antagonists has led to a general warning that Churg-Strauss syndrome may occur after taking these drugs [9,15].…”

Section: Discussionmentioning

confidence: 99%

Inhaled corticosteroids and Churg-Strauss syndrome: a report of five cases

Gall¹,

Pham²,

Vignes³

et al. 2000

Eur Respir J

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Churg-Strauss syndrome is an eosinophil-associated, small vessel granulomatous vasculitis, characterized by late onset asthma, upper airways disease, eosinophilia, and clinical manifestations of systemic vasculitis. Several cases of ChurgStrauss syndrome have been recognized in patients treated with cysteinyl leukotrienereceptor antagonists and weaned off systemic corticosteroids. These cases have led to a general warning on the possible development of Churg-Strauss syndrome after taking cysteinyl leukotriene-receptor antagonists.The authors report five cases of Churg-Strauss syndrome in severe steroid dependent asthmatics in whom inhaled corticosteroids allowed systemic corticosteroid withdrawal. It is concluded that physicians should monitor patients carefully when severe asthma is controlled with any substance allowing withdrawal from (or even avoidance) of systemic corticosteroids.Case-control studies should identify more precisely the risk factors of ChurgStrauss syndrome. Eur Respir J 2000; 15: 978±981.

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“…This fact is also supports by other steroid-sparing drugs used for asthma like theophylline, chromones, and omalizumab (anti-IgE) that apparently precipitate EGPA. An interesting study of crossed cases by Hauser et al may confirm this hypothesis [31][32][33][34]. However, a recent analysis by Bibby et al examined the association between LRA treatment and the development of EGPA in detected cases from the Reporting System Adverse Reactions FDA (Food and Drug Administration) database, and concluded that treatment with LRAs was suspected of causing EGPA in 114 cases.…”

Section: Genetic and Environmental Factorsmentioning

confidence: 99%

Churg-Strauss Syndrome or Eosinophilic Granulomatosis with Polyangiitis

et al. 2015

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Eosinophilic granulomatosis with polyangiitis (Churg-Strauss, EGPA) is a systemic small-to-medium-sized vasculitis associated with asthma and eosinophilia. Histologically EGPA presents tissue eosinophilia, necrotizing vasculitis, and granulomatous inflammation with eosinophil tissue infiltration. EGPA commonly involves the upper airway and lung parenchyma, peripheral neuropathy, cardiac disorders, and skin lesions. The anti-neutrophil cytoplasmic antibodies (ANCA) are positive in 40% of cases, especially in those patients with clinical signs of vasculitis. The pathogenesis of EGPA is multifactorial. The disease can be triggered by exposure to a variety of allergens and drugs, but a genetic background has also been described, particularly an association with HLA-DRB4. Th2 response is of special importance in the upregulation of different interleukins such as IL-4, IL-13, and IL-5. Th1 and Th17 responses are also of significance. Activated eosinophils have a prolonged survival and probably cause tissue damage by releasing eosinophil granule proteins, while their tissue recruitment can be regulated by chemokines such as eotaxin-3 and CCL17. Humoral immunity is also OPEN ACCESSSinusitis 2016, 1 25 abnormally regulated, as demonstrated by excessive responses of IgG4 and IgE. EGPA has a good respond to glucocorticoids, although the combination of glucocorticoids and immunosuppressants (e.g., cyclophosphamide, azathioprine) is needed in most of cases. Newer treatment options include anti-IL-5 antibodies (mepolizumab), whose efficacy has been described in clinical trials, and anti-CD-20, a B cell-depleting agent (rituximab), reported in several case series.

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Leukotriene antagonists and Churg-Strauss syndrome: the smoking gun

Cited by 38 publications

References 23 publications

Churg-Strauss Syndrome and Leukotriene-Modifying Agents

Churg-Strauss Syndrome and Leukotriene-Modifying Agents

Inhaled corticosteroids and Churg-Strauss syndrome: a report of five cases

Churg-Strauss Syndrome or Eosinophilic Granulomatosis with Polyangiitis

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